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A 58-year-old woman with no relevant medical history presented to the emergency department with syncope. Following a long flight 6 weeks prior, she had developed left calf tightness and pain, followed by shortness of breath for 1 week and then a syncopal event the day of admission. On physical examination, she appeared anxious, with a temperature of 36.8°C, a heart rate of 102 beats/minute, blood pressure of 128/66 mm Hg, a respiratory rate of 20 breaths/minute, and pulse oximetry of 98% on room air. Her heart and lung sounds were normal. Her laboratory results were notable for a troponin level of 0.07 ng/mL (to convert to μg/L, multiply by 1.0), and a fibrin D-dimer level of more than 2000 μg/mL (to convert nmol/L, multiply by 5.476). Her electrocardiogram on presentation showed sinus tachycardia and was otherwise normal. Computed tomography of the chest was performed, which showed multiple large bilateral pulmonary emboli (Figure, A), with deviation of the interventricular septum toward the left ventricle. Echocardiography demonstrated a large mobile thrombus extending from the right atrium into the right ventricle, as well as a clot in the left atrium and left ventricle that appeared to originate from the interatrial septum, suggesting a defect there (Video, Figure, B).
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Pulmonary embolism with patent foramen ovale and impending paradoxical embolism
C. Consult cardiothoracic surgery for controlled operative thrombectomy
Pulmonary embolus (PE) is a form of venous thromboembolism that accounts for approximately 100 000 deaths annually in the United States.1 Pulmonary emboli may be classified by severity into massive (PE causing hemodynamic compromise), submassive (PE causing right ventricular dysfunction), and nonmassive or low-risk PE, with 90-day mortality rates ranging from 58.3% for massive PE to less than 2% in low-risk PE.2 Clinical features suggestive of a poor prognosis include an elevated troponin or natriuretic peptide level, right-to-left ventricular septal bowing or right ventricular enlargement on computed tomography, and right ventricular dysfunction on echocardiography, all of which were evident in this patient.3 Treatment approaches vary by the severity of PE. Therapeutic anticoagulation with unfractionated heparin (choice A), low-molecular-weight heparin, or a direct oral anticoagulant is recommended for all acute PE, with no absolute contraindications to anticoagulation. The management of submassive and massive PEs is more complex. For patients with massive or otherwise high-risk PEs, such as this patient, the American Heart Association suggests fibrinolysis (choice D) if there is acceptably low risk of bleeding complications.4 However, either catheter embolectomy and fragmentation (choice B) or surgical embolectomy (choice C) is reasonable if fibrinolysis is contraindicated or patients remain unstable after fibrinolysis.4
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Corresponding Author: Monica M. Parks, MD, Department of Medicine, University of California, San Francisco, PO Box 0119, 505 Parnassus Ave, Room 987, San Francisco, CA 94143 (email@example.com).
Published Online: February 19, 2020. doi:10.1001/jamacardio.2019.5452
Conflict of Interest Disclosures: None reported.
Additional Contributions: We thank the patient for granting permission to publish this information.
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